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Archives of Cardiovascular Disease (2016) 109, 6780
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REVIEW
All you need to know about the tricuspid

valve: Tricuspid valve imaging and tricuspid
regurgitation analysis
Tout ce que vous avez toujours voulu savoir sur la valve tricuspide : intrts
de limagerie multi-modalits dans lanalyse de la valve et de la fuite
tricuspide
Olivier Huttin a, Damien Voilliot a, Damien Mandry b,
Clment Venner a, Yves Juillire a,
Christine Selton-Suty a,
a
Department of Cardiology, University Hospital of Nancy-Brabois, Institut lorrain du Cur et

des Vaisseaux, 54511 Nancy, France
b
Department of Radiology, University Hospital of Nancy-Brabois, Institut lorrain du Cur et
des Vaisseaux, 54511 Nancy, France
Received 1st July 2015; received in revised form 24 August 2015; accepted 27 August 2015
KEYWORDS
Tricuspid valve;
Tricuspid valve
insufciency;
Echocardiography;
Cardiac imaging;
Heart valve surgery
Summary The acknowledgment of tricuspid regurgitation (TR) as a stand-alone and progressive entity, worsening the prognosis of patients whatever its aetiology, has led to renewed
interest in the tricuspid-right ventricular complex. The tricuspid valve (TV) is a complex,
dynamic and changing structure. As the TV is not easy to analyse, three-dimensional imaging,
cardiac magnetic resonance imaging and computed tomography scans may add to twodimensional transthoracic and transoesophageal echocardiographic data in the analysis of TR.
Not only the severity of TR, but also its mechanisms, the mode of leaet coaptation, the degree
of tricuspid annulus enlargement and tenting, and the haemodynamic consequences for right
atrial and right ventricular morphology and function have to be taken into account. TR is functional and is a satellite of left-sided heart disease and/or elevated pulmonary artery pressure
Abbreviations: 2D, two-dimensional; 3D, three-dimensional; CMR, cardiac magnetic resonance; CT, computed tomography; FTR, functional tricuspid regurgitation; PAP, pulmonary artery pressure; PISA, proximal isovelocity surface area; RA, right atrium/atrial; RV, right
ventricle/ventricular; TA, tricuspid annulus; TOE, transoesophageal echocardiography; TR, tricuspid regurgitation; TTE, transthoracic
echocardiography; TV, tricuspid valve.
Corresponding author.
E-mail address: c.suty-selton@chu-nancy.fr (C. Selton-Suty).
http://dx.doi.org/10.1016/j.acvd.2015.08.007
1875-2136/ 2015 Elsevier Masson SAS. All rights reserved.
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O. Huttin et al.
most of the time; a particular form is characterized by TR worsening after left-sided valve
surgery, which has been shown to impair patient prognosis. A better description of TV anatomy
and function by multimodality imaging should help with the appropriate selection of patients
who will benet from either surgical TV repair/replacement or a percutaneous procedure for
TR, especially among patients who are to undergo or have undergone primary left-sided valvular
surgery.
2015 Elsevier Masson SAS. All rights reserved.
MOTS CLS
Valve tricuspide ;
Insufsance
tricuspide ;
chocardiographie ;
Imagerie cardiaque ;
Chirurgie valvulaire
Rsum Il est maintenant bien admis que linsufsance tricuspide (IT) signicative est une
entit propre qui aggrave le pronostic des patients, quelle que soit son tiologie, et ceci a
conduit un regain dintrt pour lensemble valve tricuspide-ventricule droit. La valve tricuspide est une structure complexe, dynamique avec une grande variabilit interindividuelle.
Les diffrentes techniques dimagerie moderne telles que lchographie tridimensionnelle,
limagerie par rsonance magntique et le scanner peuvent tre utiliss en complment de
limagerie bidimensionnelle classique pour analyser lIT. Il est important danalyser non seulement le degr de svrit de lIT, mais aussi les mcanismes son origine, le mode de coaptation
des feuillets valvulaires, le degr dlargissement de lanneau tricuspide et limportance de la
traction sur les feuillets valvulaires, ainsi que le retentissement hmodynamique sur loreillette
et le ventricule droit. LIT est dans la majorit des cas fonctionnelle et satellite dune pathologie du cur gauche et/ou dune lvation des pressions pulmonaires. LIT qui persiste et se
majore dans les suites dune chirurgie valvulaire du cur gauche est une forme particulire
ne pas mconnatre car elle pose des problmes de prise en charge et aggrave le pronostic
des patients. Une description dtaille de lanatomie et de la fonction de la valve tricuspide
et de lensemble du cur droit par limagerie multi-modalits devrait permettre dafner les
critres de slection des patients chez qui une correction de lIT doit tre envisage, particulirement parmi les patients candidats une chirurgie du cur gauche. De plus, ces lments
doivent entrer en ligne de compte dans le choix de la modalit thrapeutique optimale, savoir
rparation, remplacement valvulaire ou traitement par voie percutane.
2015 Elsevier Masson SAS. Tous droits rservs.
Background
The differences in anatomy and function between the
mitral valve and the tricuspid valve (TV) have been recognized since the anatomical descriptions of the heart by
William Harvey in 1628. Tricuspid regurgitation (TR) was rst
described by T.W. King in 1837, who showed that distension
of the right ventricle (RV) with water induced considerable
TV reux. The authors thought that the TV, being weak,
could act as a safety valve for the RV, and concluded that
the TV is designed to be(come) incompetent [1]. This
statement was accepted as true, and for a long time the TV
and TR were neglected while surgical techniques for treating left heart valvular diseases evolved. Unfortunately, TR
turned out not to be as benign and physiological as had
been thought. Some patients with progressive TR developed
intractable right ventricular (RV) failure, especially those
who had been operated on earlier for left heart valve diseases without concomitant TV surgery. These ndings led to
a renewed interest in the TV and, more globally, in the right
heart valvular-ventricular complex. Multimodality imaging
helped to better describe the morphology and function of
the TV, and to fully assess the cause and impact of TR. This
issue of TR is clinically important because it may presage a

poor prognosis, and because surgical management of TR is
far less codied than for left heart valves, and has poorer
results and frustrating failures. This review will focus on the
multimodality imaging of the normal TV, and on the pathophysiology, mechanisms and analysis of TR.
Anatomy
The TV is a complex entity of thin brous tissue, with three
leaets, chordae tendineae, papillary muscles and a brous
annulus located between the right atrium (RA) and the RV
[24]. The normal area of the TV is 79 cm2 , making it the
largest of the four cardiac valves.
Tricuspid valve leaets

The TV is nearly vertical and is oriented at approximately
45 to the sagittal plane, so that the margins of the valve
are anterosuperior, inferior and septal [5]. The three leaets
are the anterior, septal and posterior leaets, which are thin
and membranous, with commissures that appear more like
Tricuspid valve imaging and tricuspid regurgitation

indentations than true commissures. The anterior leaet is
the largest, with a semi-circular shape, and stretches from
the infundibulum anteriorly to the inferolateral wall posteriorly. The posterior leaet differs because of the presence
of multiple scallops; it attaches along the posterior margin of the tricuspid annulus (TA) from the septum to the
inferolateral wall. The septal leaet is the smallest, and
arises medially, directly from the annulus above the interventricular septum. The septal leaet is characteristically
inserted 10 mm more apically than the septal insertion of
the anterior mitral valve leaet.
Tricuspid subvalvular apparatus

The TV apparatus is similar to the mitral valve, but has
greater variability. The tricuspid subvalvular apparatus consists of anterior, posterior and septal papillary muscles,
and their true chordae tendineae. Each leaet has chordal
attachments to one or more papillary muscles. The anterior
papillary muscle, the most prominent, provides chordae to
the anterior and posterior leaets, and the medial papillary
muscle provides chordae to the posterior and septal leaets.
The anterior papillary muscle may have attachments to the
moderator band. The posterior papillary muscle is smaller,
and is missing in 20% of healthy subjects [6]. The septal wall gives chordae directly to the anterior and septal
leaets, without a specic septal papillary muscle. In addition, there may be accessory chordal attachments to the RV
free wall and to the moderator band. These multiple chordal
attachments are important mediators of TR, as they impair
proper leaet coaptation in the setting of RV dysfunction
and adverse remodelling.
Tricuspid annulus
The TV leaets are attached to a brous annulus that is
not as easy to dene as it is around the mitral valve,
although it remains identiable [7]. The septal leaet, the
least mobile of the three leaets, has more support from
the brous trigone than other leaets. The normal TA is
ovoid, and appears approximately one third longer in the
mediolateral than in the anteroposterior direction [8]. Furthermore, the TA is non-planar, with an elliptical saddle
shape. The posteroseptal portion (close to the coronary
sinus) and the anterolateral segments are the closest to
the apex and the anteroseptal (close to the RV outow
tract and the aortic valve) and posterolateral segments are
the closest to the RA, with a high-low distance of around
7 mm [9]. The mean maximal TA circumference and area
in healthy subjects are 12 1 cm and 11 2 cm2 , respectively. The TA diameter varies according to the site of
measurement, with reference values varying between 25
and 39 mm [8,9]. From a dynamic point of view, the TA shows
variability during the cardiac cycle, with an approximately
20% reduction in annular circumference with atrial systole
[10]. In pathological situations, as the septal leaet is xed
between the brous trigones, the TA can only lengthen and
dilate along the attachment of the anterior and posterior
leaets, resulting in a more circular shape; furthermore, it
then becomes more planar with decreased high-low distance
(< 4 mm) [8,9,11,12].
69
Echocardiographic imaging of the tricuspid

valve complex
Assessment of the TV using transthoracic echocardiography
(TTE) is challenging because of its unfavourable retrosternal position, the high variability of the TV anatomy and
the difculty in simultaneously visualizing all three leaets
in standard two-dimensional (2D) views; hence, all existing echocardiographic TV leaet identication schemes are
only partially correct. The use of an en-face view obtained
by 2D TTE or, more easily, by transoesophageal echocardiography (TOE) and three-dimensional (3D) imaging is therefore
recommended [13,14].
Tricuspid valve morphology

TV morphology can be evaluated by 2D TTE from the
standard parasternal and apical RV views: RV inow,
parasternal short-axis, apical four-chamber and subcostal
views (Fig. 1). It is important to use all available views
in 2D, colour and Doppler modes to obtain a complete
evaluation of the valve by 2D TTE, and to rule out and
not underestimate a ail leaet or a localized abnormality. TOE helps to image the TV in multiple views
and planes, although the incremental value of TOE is
usually less for the TV than for the mitral valve. The
deeper gastric view in a longitudinal plane (transgastric
RV inow view) often provides a nice long-axis visualization of the TV and the subvalvular apparatus. An en-face
view is also quite easily obtained from the gastric approach
(Fig. 2).
Finally, 3D imaging is used mostly in TTE, from either
the parasternal or the apical approach, with real-time zoom
mode or after acquisition of a full-volume data set; this
allows the display of the TV surgical view and visualization of all the components of the TV, enabling assessment
of their dynamic spatial relationships and anatomical continuity [1416] (Fig. 3). In patients with good echogenicity,
assessment of TV anatomy and function with 3D TTE is often
feasible, even if it is more difcult and requires more experience compared with mitral valve 3D evaluation [14]. 3D
TTE has the potential advantage of evaluating complex TV
anatomy in organic TR, as may be encountered in Ebsteins
anomaly, carcinoid heart disease and TV prolapse [1719].
Recently, several publications have highlighted the usefulness of 3D TTE for detecting the location of the lead and its
relationship to valvular leaets and signicant TR in patients
with intracardiac devices [2022]. 3D TTE also enables us to
locate the anatomical regurgitant orice of TR and to measure the vena contracta, which was found to be more often
ellipsoid than circular [23]. Finally, the extent of TV tethering may be quantied with 3D echocardiography, in terms of
the tenting volume and tenting angle of the three leaets
[24,25].
Tricuspid annulus
TA size and function play pivotal roles in the genesis of TR,
and accurate analysis of the TA is required to determine the
need for a combined procedure on the TV in patients undergoing cardiac surgery for left-sided valve diseases. However,
70
O. Huttin et al.
Figure 1. Two-dimensional transthoracic imaging of the tricuspid valve. RV: right ventricle; TV: tricuspid valve; AL: anterior leaet; PL:
posterior leaet; SL: septal leaet.
normative data about TA diameter and function are limited,

and are still a matter of debate.
As for the description of TV morphological details, 2D
TTE has some limitations in the quantication of the TA
diameter [26,27]. In fact, the 2D view and the timing
during the cardiac cycle of when the TA should be measured
remain controversial [10]. If 2D TTE is the only assessment

tool available, the apical four-chamber view seems to
be preferred, because of better interobserver agreement
compared with other views [28], and it is the method
recommended by current guidelines for making a decision
about TV repair [29,30]. In this view, the normal TA diameter
71
Figure 2. Two-dimensional transoesophageal imaging of the tricuspid valve (TV). RV: right ventricle; TV: tricuspid valve; AL: anterior
leaet; PL: posterior leaet; SL: septal leaet.
in adults is 28 5 mm, measured in diastole. The TA can

also be measured from the mid-oesophageal four-chamber
view in 2D TOE (Fig. 4).
To assess cyclic changes in TA diameter during systole and
diastole, TA fractional shortening may be calculated from
the apical four-chamber view between the insertion sites
of the septal and anterior TV leaets at end-diastolic and
end-systolic times; the normal value is around 25% [28].
The analysis of TA geometry and size with the use
of 3D echocardiography shows interesting results and
has good feasibility [8,9,11,29,3134] (Fig. 4). Various
measurements are reported, including major and minor TA
diameters, TA fractional shortening, TA area and TA fractional area change. TA diameter is usually underestimated
by 2D TTE compared with 3D TTE, and it seems necessary
to re-establish normal TA values with 3D imaging. Furthermore, more complicated analysis of the non-planarity
of TA can also be performed from 3D acquisitions, which
have potentially important mechanistic and therapeutic
implications for TV repair [8,11].
Value of other imaging modalities in the

assessment of the tricuspid valve
Electrocardiograph-gated computed tomography (CT) scans
and cardiac magnetic resonance (CMR) imaging are interesting adjuncts in the evaluation of the TV.
Computed tomography scans

The dynamic data set acquired in patients who undergo CT
scans can be used to assess RV function. The thin slice thickness facilitates increased accuracy of RV delineation, and
allows for precise recognition of the valvular borders. For
the TV, only static anatomical information is relevant [35].
Measurements of TA diameter and assessment of lack of
coaptation of leaets are generally simple on good-quality
four-chamber cardiac CT images (Fig. 5). Evaluation of TV
prolapse is easier on coronal views. In functional TR (FTR),
CT scans have been used to measure right atrial (RA) and
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O. Huttin et al.
Figure 3. Three-dimensional (3D) imaging of the tricuspid valve (TV). RV: right ventricle; TV: tricuspid valve; AL: anterior leaet; PL:
posterior leaet; SL: septal leaet; RT3DE: real-time 3D echocardiography.
RV volumes, TA diameters and areas, the distance between

each commissure, the tethering angle of each leaet and the
tethering height, with these various indexes having interesting prognostic value [36,37]. Some other potential benets
of CT scans are the detection of valvular calcications, the
evaluation of TV annuloplasty ring dislodgement and the
assessment of the spatial relationship between RV pacemaker leads and related TR [35].
Cardiac magnetic resonance imaging

With its ability to image in any plane, CMR can provide
detailed characterization of all valvular structures [38,39].
Most morphological and functional information is obtained

using cine CMR sequences, particularly steady-state free
precession sequences. In addition to echocardiography, CMR
is the technique of choice for evaluating tricuspid abnormality [40]. As for CT scans, 2D measurements of annulus
diameter, tethering height and lack of coaptation of leaets
with direct planimetry of the valvular orice area are feasible using the different sequences focused on the RV (Fig. 5).
A semiautomatic algorithm based on cine CMR images and
3D reconstruction can help to assess TA morphology and
motion and to better depict its ellipsoid saddle shape [41].
TA dynamics have, in this way, been shown to be minimal in
the anteroseptal region and maximal in the posterior region
73
Figure 4. Tricuspid annulus (TA) diameter assessment by two-dimensional (2D) and three-dimensional (3D) transthoracic echocardiography.
(Top) 2D apical four-chamber and subcostal long-axis view with end-diastolic TA measurement. (Bottom left) Volume rendering of the TA
shown from the right ventricular perspective. The laser lines superimposed on the 3D echocardiography rendering indicate the orientation
of the corresponding depicted image in the longitudinal 2D views of the tricuspid valve. (Bottom right) Measurements of diameters from
the end-diastolic 3D frame of the TA.
[42]. Finally, CMR is currently the gold standard for the

assessment of RV morphology and function, and is therefore
of great interest in the eld of TR.
Tricuspid regurgitation
TV function depends on interactions between the TA, valvular leaets, papillary muscles, chords, the RA and the RV. Any
congenital or acquired abnormality affecting one of these
structures leads to TR.
Epidemiology
Mild physiological TR is very frequent and well known
by echocardiographers who, by applying the simplied
Bernoulli formula, use its maximal velocity to estimate systolic pulmonary artery pressure (PAP) [43]. Depending on
the series, physiological TR is reported to be present in
6090% of people who undergo echocardiography, and its
incidence increases with age. TR is mostly trivial or mild. In
the Framingham study, the prevalence of mild or greater TR
by colour Doppler was 15% in men and 18% in women [44].
In a large database of more than 60,000 echocardiograms,
TR was reported to be severe in only 1.2% of patients [45].
It is estimated that moderate-to-severe TR affects approximately 1.6 million patients in the USA [7].
cardiac pathology). Some authors also individualize idiopathic TR (normal TV and no aetiology identied for TR)
[46]. In a series of 768 cases of severe TR, organic TR and
FTR represented 11% and 80% of the cases, respectively, and
idiopathic TR accounted for 9%, with these patients being
older and having a higher frequency of AF than the others
[45]. Carpentiers classication based on the amplitude of
valvular displacement (normal for type 1, excessive for type
2 and restrictive for type 3) can also be applied to describe
the mechanisms of TR (Table 1).
Pathophysiology
TR is responsible for progressive RA dilatation, increased
pulsatility and dilatation of the inferior vena cava and
hepatic veins, coronary sinus dilatation and septal shift
towards the left atrium. Whatever the initial mechanism, TR
also leads to RV volume overload and increased RV diastolic
pressure, septal shift towards the left ventricle and increasing RV dilatation, with displacement of papillary muscles and
leaet tethering, decreased amplitude of leaet motion and
valvular tenting further impairing valvular coaptation. This
vicious circle progressively increases TR and decreases cardiac output, leading to nal RV failure. In addition, atrial
brillation, which often complicates all these pathologies,
leads to a further annular dilation (Fig. 6).
Aetiologies and mechanisms
Symptoms
As for the mitral valve, the aetiology of TR is divided into

organic TR (TV pathology) and FTR (secondary to other
In advanced stages of TR, there is the progressive appearance of venous dilation, with signs of right-sided heart
74
O. Huttin et al.
Figure 5. Cardiac magnetic resonance (CMR) imaging and computed tomography (CT) scans of the tricuspid valve (TV). RV: right ventricle;
TV: tricuspid valve; AL: anterior leaet; PL: posterior leaet; SL: septal leaet; SV: stroke volume; HLA: horizontal long-axis; SSFP: steadystate free precession cine MRI; MinIP: minimal intensity projection.
failure, such as congestive hepatopathy, loss of appetite,

ascites, gut congestion with symptoms of dyspepsia or feeling of abdominal fullness and uid retention with peripheral
oedema. Furthermore, the decrease in cardiac output is
responsible for fatigue, exertional dyspnoea and decreased
functional capacity [27,47,48].
Organic/primary tricuspid regurgitation

Organic TR results from structural abnormalities of the
valvular apparatus, which are either congenital or acquired.
Table 1 summarizes the main causes and mechanisms of
non-congenital organic TR. Some recent reports insist on

Table 1
75
Causes and mechanisms of tricuspid regurgitation.
Organic
Functional
Type 1
Type 2
Type 3
Type 1/
Endocarditis (perforation)
Congenital (cleft leaet)
PM leads
Degenerative (prolapse)
Endocarditis (ruptured
chordae)
Traumatic (ruptured
chordae)
Rheumatic iatrogenic
(radiation/drug)
Carcinoid
PM leads
Left heart disease (valvular,

myocardial)
Left-sided valve surgery
Primitive RV dysfunction
(cardiomyopathy, ischemic)
Secondary RV dysfunction/dilation
(PAH, pulmonary diseases)
a peculiar form of TR related to stimulation device leads

(pacemaker, cardiac resynchronization therapy, implantable
cardioverter debrillator). Those leads have been reported
to cause TR of variable degree. With the help of 3D echocardiography, a clear association between device lead position
and TR was found, regurgitation being more frequent when
the leads are impinging on the leaets and interfering with
their mobility than when placed in a commissural position
[22]. Furthermore, the presence of an interfering lead is a
factor associated with TR worsening, increasing the likelihood of developing moderate or severe TR by more than
10-fold [20].
Functional/secondary tricuspid regurgitation

FTR is dened as the leakage of the TV during systole in
the presence of structurally normal leaets and chordae.
Nevertheless, in case of signicant TR, it entails abnormalities of the valvular apparatus, with tricuspid annular dilation
and tricuspid leaet tethering secondary to RV dilation and
dysfunction [49].
Dilation of the TA occurs primarily in the septolateral
direction, resulting in a less oval orice [50]. 3D echocardiography has determined that not only dilation, but also
modications of the structure of the TA exist in FTR patients,
Figure 6. Pathophysiology of tricuspid regurgitation. ARVD: arrhythmogenic right ventricular dysplasia; LA: left atrial; LV: left ventricular;
RA: right atrial; RV: right ventricular.
76
O. Huttin et al.
with a more planar TA than in healthy subjects [8,11]. Loss

of longitudinal exibility and more restricted movement of
the TA have also been shown by CMR in the early stages of
FTR, resulting in leaet tethering even in the absence of
RV dilation [51]. Leaet tethering following displacement
of papillary muscles caused by progressive RV distortion and
eccentricity also inuence the development of FTR [7]. All
these mechanisms are variously implicated in the development of FTR. For instance, Topilsky et al. showed that
in idiopathic FTR, excess annular and RV inow enlargement exhausts valvular/annular coverage reserve, and RV
conical deformation does not cause notable valvular tenting. Conversely, in pulmonary hypertension, FTR is mostly
determined by valvular tethering, with tenting linked to RV
elongation and elliptical/spherical deformation [52].
The most common cause of FTR is left heart disease,
including advanced mitral, aortic and/or left ventricular
myocardial disorder. FTR may also complicate either pulmonary (pulmonary diseases, pulmonary hypertension) or
intrinsic (RV cardiomyopathy, arrhythmogenic RV dysplasia,
RV infarction, endomyocardial brosis, etc.) RV myocardial
diseases (Fig. 6). Elevated PAP is a strong determinant of
the presence of signicant TR and of TR severity, although
many patients with pulmonary hypertension do not exhibit
signicant TR [53]. So, more than just the absolute value
of the PAP, remodelling of the right heart in response to
elevated PAP and its causes is one of the factors at the origin of FTR. In a large series of more than 2000 patients
who had TR-derived estimation of PAP, demographic characteristics (age, female sex), mechanical factors (presence
of pacemaker leads), remodelling of the right heart cavities (RA, RV enlargement) and other factors (e.g. organic
mitral valve disease, possibly reecting the presence of
atrial brillation or occult organic TV disease) were predictive of TR severity in addition to PAP [54]. In a case-control
study on the follow-up of patients with mild TR, progressive
increase in PAP, atrial brillation and coronary artery disease were independent predictive factors of TR progression
[55].
Functional tricuspid regurgitation in the

follow-up of left heart valve surgery
One peculiar form of FTR complicating left heart diseases
is represented by FTR appearing in the follow-up of leftsided valve surgery; this is quite frequent after mitral valve
surgery and may occur whatever the type of procedure
(repair or replacement) or valvular substitute (biological or
mechanical). Until recently, it was believed that surgical
correction of left-sided lesions would lead to the disappearance of secondary TR. However, if not treated during the
initial surgery, pre-existing FTR may persist and worsen over
time. In the presence of severe TR associated with degenerative mitral valve disease, mitral valve repair alone leads to
improved TR and RV function; however, this improvement is
incomplete and temporary, and TR and RV function worsen
toward preoperative levels within 3 years [56]. Moreover,
late occurrence of signicant TR long after the initial surgical procedure has been shown to be quite common after
mitral surgery, and is associated with a poor prognosis in
terms of morbidity and mortality [57].
Many factors inuencing the occurrence of signicant TR

during the follow-up of mitral surgery have been reported:
older age, female sex, rheumatic fever as the origin of
mitral dysfunction, long period of valvular disease before
surgery, atrial brillation, level of preoperative PAP and
preoperative RV dysfunction. Furthermore, preoperative TA
dilation [58,59] and the tethering height and tenting volume of TV are important independent predictors of late TR
[36].
The type of underlying mitral disease justifying initial
surgery probably also plays a role in the occurrence of signicant TR. TR seems to be more frequent in case of initial
surgery for ischaemic MR, reported as being as high as 74%
after 3 years of follow-up [60], than in case of surgery for
organic MR, where < 20% of patients had severe TR after a
8-year follow-up period [61]. It has even been reported that
clinically-silent non-severe TR is unlikely to progress after
mitral valve repair for degenerative prolapse [62]. However, these discrepancies between ischaemic and organic
origin of initial mitral valve disease are the result of unclear
mechanisms [63]; concomitant RV dysfunction in ischaemic
diseases probably plays a role in the higher late occurrence
of signicant TR.
FTR is also seen in patients with aortic stenosis, persisting in a signicant degree after valvular replacement in
around 15% of the patients, with a further progression in half
of these patients. As for the mitral valve, persistent FTR
greater than mild was associated with a worse long-term
prognosis [64].
Relationship between tricuspid regurgitation

and right ventricular function
The relationship between TR and RV function is complex. RV
dysfunction mostly inuences TR severity through RV remodelling [65]. The inuence of severe TR on RV function is less
clear.
Experimentally, it has been shown that severe TR in
dogs leads to pump failure, but without cellular contractile
dysfunction, suggesting a relative preservation of intrinsic
RV contractile function despite severe TR [66]. Likewise,
old series of tricuspid valvulectomy have shown relatively
good tolerance at mid-term follow-up in around twothirds of patients, without signs of congestive heart failure
[67,68].
On the other hand, echocardiographic variables of RV
function have been shown to alter in parallel with the
increase in TR severity [69]. The effect of TR on RV function variables varies according to the mechanisms of TR,
but signicant TR always leads to increased end-systolic
RV size and RV myocardial performance index in both idiopathic FTR and FTR secondary to pulmonary hypertension,
with an additional decrease in RV fractional area change in
idiopathic FTR, and an increase in RV end-diastolic area in
FTR secondary to pulmonary hypertension, suggesting universally reduced RV function with increasing FTR severity
[52].
Finally, RV function seems to improve after correction
of isolated TR [70], with a reduction in RV volumes [40];
this is also the case when mitral and tricuspid surgery are
combined [56]. In the same manner, it has been shown

that the degree of both RV dysfunction and TR severity improves after pulmonary endarteriectomy in chronic
thromboembolic pulmonary hypertension [71,72]. These
studies suggest that severe TR leads to RV dysfunction; however, RV function seems, in some cases, to improve after
surgical treatment of either TR or the aetiology of increased
RV afterload that is responsible for TR. The real challenge
is actually to correctly identify patients whose RV function
is deemed good enough for the heart to take advantage of
a competent TV [73].
The main issue is that echocardiographic variables of RV
function and even CMR-derived RV ejection fraction are well
known to be load dependent and not to be a proper reection of intrinsic RV contractility [74,75]; the real impact
of severe TR on intrinsic RV contractile function and on
its potential reversibility is therefore difcult to assess.
Furthermore, it has been shown that echocardiographic
variables of RV function may be altered in the follow-up
of cardiac surgery, even in the absence of real RV dysfunction, so that the true impact of TR correction on RV function
is also very difcult to comprehend [76,77]. Nevertheless,
preserved RV function variables in the presence of signicant TR are always associated with a better prognosis than
altered ones [56,78,79].
Echocardiographic analysis of tricuspid

regurgitation
As for every other valve, the echocardiographic analysis
of TR encompasses a description of TV morphology, quantication of TR and the assessment of its haemodynamic
consequences.
The quantication of TA enlargement, the mode of leaet
coaptation and the degree of tenting are of utmost importance when making a surgical decision about TV repair or
replacement. Signicant TA dilatation is dened by a diastolic diameter 40 mm or > 21 mm/m2 in the four-chamber
transthoracic view, and is considered as a criterion for
concomitant tricuspid procedure in case of left-sided valve
surgery [29]. Dreyfus et al. classied the mode of leaet
coaptation as body-to-body in case of normal coaptation,
as edge-to-edge or edge-to-body in case of symmetric or
asymmetric abnormal coaptation, and as lack of coaptation
in case of gaping valve [80]. Quantication of the degree of
leaet tethering needs measurement of the coaptation distance and the tenting area [9]. Coaptation distance > 8 mm
and tenting area > 1.6 cm2 characterize signicant tethering.
Measurements of tenting volume and tenting angles from 3D
views have also been reported to independently determine
residual TR after tricuspid annuloplasty [24].
When quantifying TR, echocardiographers must always
remember the marked RV plasticity with inspiratory and
loading changes, and bear in mind the resulting potential variations of TR over time, on a short-time scale for
respiratory variations and on a longer time scale for variations caused by different loading conditions. Topilsky et al.
nicely showed augmentation of TR during inspiration. The
inspiratory increase in regurgitant orice area is explained
by inspiratory annular enlargement and RV shape widening, resulting in decreased valvular coverage and increased
valvular tenting [81]. In the same manner, RV morphological
77
changes with preload and afterload variations imply potential variability of TR over time. So, echocardiographic
analysis of TR should always take place after medical optimization of loading conditions, and rely on multiple TR
measurements averaged over the respiratory cycle.
Grading the severity of TR is not an easy task. There
is general agreement about trivial/mild TR seen in different views by colour Doppler as a small central regurgitant
blue jet. However, the sole use of colour ow imaging to
quantify higher grades of TR is not recommended, as it
is limited by several technical and haemodynamic factors.
Nevertheless, large eccentric jets, swirling and reaching
the posterior wall of the RA, usually indicate signicant
TR [82]. Scientic societies in Europe and the USA have
published recommendations for the quantication of TR
[29,30,82,83]. According to the European guidelines and
many experts [47,80], TR should be quantied in three
grades (mild, moderate and severe) using the classical variables of vena contracta width, regurgitant orice area and
regurgitant volume calculation by the proximal isovelocity
surface area (PISA) method, and analysis of anterograde and
regurgitant ow proles and hepatic vein ow. However, all
these variables are less robust and have been less validated
for TR than for MR. Furthermore, the shape of the regurgitant orice is more frequently stellar or ellipsoid than
circular in TR, and multiple jets are frequent, disqualifying the use of most of these variables. Nevertheless, there
is quite a consensus for the denition of severe TR (triangular ow with early peak, E tricuspid velocity > 1 m/s, vena
contracta > 7 mm, PISA regurgitant orice area > 40 mm2 ,
regurgitant volume > 45 mL and systolic reversal of hepatic
ow), but the boundaries between mild and moderate TR
remain poorly dened.
Finally,
echocardiography
also
evaluates
the
haemodynamic consequences of TR, with the analysis
of the inferior vena cava, and RA and RV size and function.
However, right heart chamber dilatation and RV dysfunction
may not only be the consequence, but also the cause of
TR, and must be interpreted with special attention to
pulmonary haemodynamics and clinical context.
Cardiac magnetic resonance analysis of

tricuspid regurgitation
On in-plane balanced steady-state free precession or phase
contrast cine imaging, the regurgitant ow is shown on CMR
as a triangular jet into the RA, but the TR jet may be difcult
to evaluate because of low turbulence. Obtaining a shortaxis image orthogonal to the jet ow is the ideal means of
acquiring information about the velocity and direction of
ow. Therefore, the jet of regurgitation, especially when it
is mild, can be better shown by gradient-recalled echocardiography imaging. TR is best imaged in the four-chamber
view and the coronal oblique view displaying the RA and the
RV. A vena contracta > 7 mm classies TR as severe [8486].
TR can also be quantied in terms of regurgitant volume and fraction in similar ways to mitral regurgitation:
the forward stroke volume, as measured in the pulmonary
artery with phase contrast, is subtracted from the total
RV stroke volumes from the steady-state free precession
images or from the difference in right-left ventricular stroke
78
O. Huttin et al.
volumes [87]. However, this method is not applicable in case

of irregular rhythms or signicant other valve regurgitation.
Natural history and prognostic implications

Many studies have underlined the poor prognosis associated with severe TR. In a recent study of 350 patients
with isolated TR, the 10-year survival rate was lower with
an regurgitant orice area > 40 mm2 vs. < 40 mm2 (39% vs.
71%), independent of all characteristics, RV size or function,
co-morbidity or pulmonary pressure, and was lower than
expected in the general population [88]. In the follow-up
of 200 patients with mild TR, all-cause mortality at 3 years
was 20% for patients without TR progression, 42% for moderate TR and 63% for severe TR, and progression to severe
TR independently predicted subsequent mortality [55]. Similar results have been found in the follow-up of left-sided
heart valve surgery, with a better prognosis and improved
long-term right-sided remodelling in patients who undergo
concomitant tricuspid annuloplasty [89], and a poorer prognosis in patients with residual and/or late progression of TR
[57,90]. Furthermore, in those patients, there is high morbidity and mortality associated with reoperative open-heart
surgery, partly as a result of the unpredictable evolution of
the RV [91]. So, a combined procedure on TR at the time
of surgery is increasingly supported by published guidelines,
despite the lack of randomized data proving its benet [92].
Conclusion
Increased mortality among patients with TR, regardless of
pulmonary pressure, RV function or left heart valve disease
has revived interest in the TV. The optimal analysis of the
TV should be achieved through a perfect knowledge of its
anatomy, function and pathophysiology, and through a thorough evaluation with multimodality imaging. 2D, 3D TTE
and TOE, together with CT scans and CMR, allow the accurate morphological description of the TV complex, including
leaets, subvalvular apparatus and the TA, and quantitative
evaluation of TR and RV function. However, the selection of
patients who will benet from surgical repair or replacement
of the TV, either in isolation or combined with another surgical procedure on the left heart, is a subject of hot debate in
the eld of heart valve disease, and the development of new
percutaneous procedures further adds to the complexity of
this issue.
Disclosure of interest
The authors declare that they have no competing interest.
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Archives of Cardiovascular Disease (2016) 109, 6780

All you need to know about the tricuspid

Department of Cardiology, University Hospital of Nancy-Brabois, Institut lorrain du Cur et

issue of TR is clinically important because it may presage a

Tricuspid valve leaets

Tricuspid valve imaging and tricuspid regurgitation

Tricuspid subvalvular apparatus

Echocardiographic imaging of the tricuspid

Tricuspid valve morphology

normative data about TA diameter and function are limited,

remain controversial [10]. If 2D TTE is the only assessment

Tricuspid valve imaging and tricuspid regurgitation

in adults is 28 5 mm, measured in diastole. The TA can

Value of other imaging modalities in the

Computed tomography scans

RV volumes, TA diameters and areas, the distance between

Cardiac magnetic resonance imaging

Most morphological and functional information is obtained

Tricuspid valve imaging and tricuspid regurgitation

[42]. Finally, CMR is currently the gold standard for the

Aetiologies and mechanisms

As for the mitral valve, the aetiology of TR is divided into

failure, such as congestive hepatopathy, loss of appetite,

Organic/primary tricuspid regurgitation

Tricuspid valve imaging and tricuspid regurgitation

Causes and mechanisms of tricuspid regurgitation.

Left heart disease (valvular,

a peculiar form of TR related to stimulation device leads

Functional/secondary tricuspid regurgitation

with a more planar TA than in healthy subjects [8,11]. Loss

Functional tricuspid regurgitation in the

Many factors inuencing the occurrence of signicant TR

Relationship between tricuspid regurgitation

Tricuspid valve imaging and tricuspid regurgitation

Echocardiographic analysis of tricuspid

Cardiac magnetic resonance analysis of

volumes [87]. However, this method is not applicable in case

Natural history and prognostic implications

Tricuspid valve imaging and tricuspid regurgitation

three-dimensional echocardiography and magnetic resonance

[60] Matsunaga A, Duran CM. Progression of tricuspid regurgitation

chronic degenerative mitral regurgitation. Ann Thorac Surg

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